Abstract
Re-exposure to either palatable food or to conditioned stimuli associated with food is known to reinstate food-seeking after periods of abstinence. The nucleus accumbens core and shell are important for reinstatement in both food- and drug-seeking paradigms, although their potential differential roles have been difficult to delineate due to methodological differences in paradigms across laboratories. The present studies assessed the effects of temporary inactivation of the core or shell on priming- and cue-induced reinstatement of food-seeking in identically-trained rats. Inactivation of either the nucleus accumbens core (Experiment 1A; N = 10) or medial shell (Experiment 1B; N = 12) blocked priming-induced reinstatement in an equivalent manner. Similarly, inactivation of the core or medial shell (Experiments 2A & 2B; N = 11 each) also blocked cue-induced reinstatement, although there was also a significant treatment day X brain region X drug order interaction. Specifically, rats with core inactivation reinstated lever-pressing on the vehicle injection day regardless of whether that was their first or second test, whereas rats that had medial shell inactivation on the first day did not significantly reinstate lever-pressing on the second day of testing (when they received vehicle). Yohimbine, while a reportedly robust pharmacological stressor, was ineffective at inducing reinstatement in the current stress-induced reinstatement procedure. These data suggest that both the nucleus accumbens core and shell serve important roles in reinstatement of food-seeking in response to priming and cues.
Highlights
According to the Centers for Disease Control, over 35% of the adult US population is obese
Despite efforts that target weight loss by changing dietary habits, most people relapse to their previous eating habits within a few months [3]
Active lever responding was analyzed with a 2 X 2 X 3 mixed ANOVA, with brain region, drug order, and treatment day as the independent variables
Summary
According to the Centers for Disease Control, over 35% of the adult US population is obese. Numerous studies suggest that dietary relapse is often influenced by re-exposure to previously avoided foods [4], exposure to cues associated with the avoided foods [5], or exposure to stressful life events [6,7]. Studies of animal reinstatement of reward-seeking behavior have been increasingly employed as a means to study the neural mechanisms involved in relapse to food-seeking behavior. The reinstatement paradigm is used to model human relapse to drug- or food-seeking [8,9,10] and allows for the potential of independently manipulating the availability of cues predicting food, the availability of the food itself (priming), or the physiological (stress) state of the animal
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